Electroanatomic Mapping of the Atrioventricular Node and Right Inferior Nodal Extension: Insights from a Case Series

The electrical activity of the atrioventricular (AV) node, and its extensions, can be mapped in the electrophysiology laboratory in humans.^1–3 Reports on 3D electroanatomic mapping of the AV node, and associated structures specifically, are less frequently encountered in the literature. The right inferior nodal extension, which represents the anatomical substrate of the slow pathway, is activated both during sinus rhythm and during AV nodal re-entrant tachycardia (AVNRT).⁴ We hypothesised that, guided by well-defined anatomical landmarks, we can apply high-resolution 3D electroanatomic mapping techniques to characterise the electrical activity of the AV node and its right inferior extension during sinus rhythm in patients referred for catheter ablation of typical AVNRT.^5,6

Methods

Patients

Three patients referred for ablation of typical AVNRT were recruited to undergo 3D electroanatomic mapping of the triangle of Koch during sinus rhythm. The study protocol received institutional review board approval, and all patients provided informed, written consent.

Mapping Procedure

Patients were studied in the post-absorptive state, under mild sedation and after cessation of all anti-arrhythmic medications for at least two half-lives. Femoral venous access was obtained using standard approaches, and electrophysiology catheters were positioned in the high right atrium, His, coronary sinus and right ventricular apex. 3D electroanatomic mapping of the triangle of Koch during sinus rhythm was performed before any ablation of AVNRT was attempted. Mapping performed after electrophysiological study, using standard manoeuvres as described previously, confirmed a diagnosis of typical AVNRT.⁷

Electroanatomic Mapping and Anatomical Landmarks

3D electroanatomic mapping was performed with the Orion catheter combined with the Rhythmia HDx SW 4.0 (Boston Scientific) system, with the use of a high-bandpass filter of 30–300 Hz for bipolar and 1.0–300 Hz for unipolar mapping. This basket catheter has 64 electrodes of 0.9 × 0.45 mm ring electrode size and 1.6 mm spacing.⁸ In anatomical terms, the distal extent of the node is posterior and inferior to the site of the catheter recording the His potentials. This can be defined by withdrawing the His recording catheter back such that it first records only the atrial and His potentials and then fails to record a His potential. In this way, using the mapping catheter, it is possible to identify the location of the AV node relative to the non-branching bundle. When mapping the zone of the non-branching bundle, a His potential can be recorded in more than one discrete location in the area.⁹ This is due to the fact that the non-branching component of the conduction axis was shown to be 3.6 ± 1.7 mm in length.¹⁰ The approximate location of the AV conduction axis relative to the landmarks of the right side of the septal structures using gross dissection has also been revisited recently.⁵ The distance between the compact node and the septal isthmus has been measured at approximately 4 cm.¹¹ The AV node is the proximal right atrial portion of the conduction axis that electrically connects the atria to the ventricles. The node has a length varying between 5 mm and 7 mm, and a width between 1.0 mm and 1.5 mm.¹²

Results

All patients studied had typical AVNRT documented during routine electrophysiology study prior to 3D electroanatomic mapping of the triangle of Koch. All patients had structurally normal hearts on transthoracic echocardiography. The mean age was 50.0 ± 9.8 years and two patients were female.

3D Electroanatomic Mapping

Detailed 3D electroanatomic mapping on the septal area that corresponds to the anticipated anatomical site of the AV node, as described in the Methods, was accomplished during sinus rhythm in all patients. Electrical activity at this site, by means of high-frequency signals following the atrial electrogram, was recorded in all patients. This ‘biphasic’ electrogram was taken as indicative of the conduction axis, and possibly the non-branching His bundle.

Once a His bundle potential was recorded the Orion catheter was withdrawn towards the areas of the AV node (Figure 1). Despite a perturbation of the recording, we could not ascertain a clearly detectable signal at bipolar mapping. Unipolar mapping, however, identified a low-frequency, low-amplitude recording that is compatible with nodal activity in all three patients (Figure 2).

Further withdrawal of the Orion towards the lower part of the triangle of Koch identified another sharp unipolar potential that may represent activation of the right inferior nodal extension (Figure 3). Results were consistent in all three patients mapped.

It is also worth noting that both the sharp bipolar deflection seen in Figure 2 and the lower frequency unipolar potential seen in Figure 3 occur early with respect to the His potential seen in Figure 1. This was the case in all patients studied.

Discussion

From our case series of 3D electroanatomic mapping during sinus rhythm, and in the triangle of Koch, in patients undergoing catheter ablation of AVNRT we can make two main observations.

First, we were able to record a sharp unipolar electrogram with a steep dV/dt that is unlikely to originate in the slowly conducting specialised myocardium of the compact AV node in all three patients studied. Our findings are in keeping with those of Pandozi et al.² We postulate that these sharp components may be indicative of the right inferior nodal extension. It is now known that the left inferior extension is capable of mainly slow conduction. The right inferior extension is capable of both slow and fast conduction. These differences may be in part due to the varying embryonic origin of the tissues. The right inferior extension originates from AV canal myocardium while the left, from a combination of AV canal myocardium and the atrial component of the primary ring. This notion is also supported by connexin genotyping studies.⁴ Thus, these potentials might originate in the right inferior nodal extension that, during sinus rhythm with conduction through the ‘fast’ pathway, the last atrial input, may be active as a bystander.⁴ Nonetheless, the right inferior extension remains a controversial structure. Although immunohistochemistry of the proposed right inferior extension indicates that it has high levels of connexin 43 expression (and therefore is able to conduct rapidly), this claim is not universally acknowledged.¹³ Some authors have speculated that the right inferior extension may indeed be a lower nodal bundle.^13–15 However, the existence of a lower nodal bundle is also in and of itself questionable. Our study is unable to provide evidence to de-mystify these issues, however, we do demonstrate rapid activation in the anatomical area of the right inferior extension by recording the bipolar electrogram shown in Figure 3. Another explanation for the sharp component we identified could be due to atrial tissue conduction heterogeneities.

Second, we used unipolar mapping with bandpass filtering of 1.0–300 Hz, to identify a low-frequency recording that might be interpreted as activation of the AV node itself. We identified this unipolar deflection shown in Figure 2 in two of our patients. The electrical activity of the node itself cannot be recorded in humans using conventional standard electrodes, despite initial reports of an extracellular nodal potential in animals, and also identification of the region of the AV node with the use of microelectrode-embedded catheters that more accurately define the near-field compact AV node compared with conventional catheters.^16–18 The difficulties in recording the nodal potential are related to the low mass of nodal tissue, slow conduction velocity causing lower amplitude electrograms, and the size and spacing of the catheters used for ablation. In addition, the node is relatively deep in the pyramid of Koch, being covered by a layer of working atrial myocardium. Thus, the signal from the node will be mixed with the potentials recorded from the overlying working atrial cardiomyocytes. Recently, Pandozi et al. reported recording the nodal activity with the Orion catheter, which has small inter-electrode spacing, and bipolar electrogram filtering at 0.50–300 Hz, and with the use of specific filter settings.^1,2 We have been unable to reproduce this result with bipolar mapping, perhaps due to the lower setting of our filters (30–300 Hz). In our study, we opted to use unipolar recordings with a lower bandpass filter to increase the mapping field of view to attempt to identify the electrical activity of the AV node that is a deeper, more insulated structure, the activation of which may evade bipolar electrogram mapping. The AV node is a very slow conducting tissue with reported conduction velocities of 0.02–0.1 m/s in humans, as opposed to 1.2–2.0 m/s in the His bundle.^19–21 Thus, a very low-frequency signal is perceivable in this respect. Given that we could not detect a nodal potential at bipolar mapping, no atrial pacing to verify the origin of the recorded potential at achieved Wenckebach conduction with loss of ventricular stimulation was performed. Our results indicate that mapping the electrical activity of the right inferior nodal extension in humans is feasible in the electrophysiology laboratory.

Limitations and Conclusion

First, this study was a small case series of only three patients. Therefore, any results are difficult to generalise. Additionally, we had planned to interrogate the triangle of Koch using only 3D electroanatomic mapping. We did not perform specific pacing manoeuvres to elucidate the electrophysiology of the area in more detail. As such, our results provide only observations that should serve as hypothesis-generating ideas. Further and larger studies are required to elucidate the electrophysiology of the conduction system axis during sinus rhythm in patients with structurally normal hearts.